Changes in the immunoreactivity of protein gene product (PGP) 9.5 in the cochlea of spontaneously diabetic WBN/Kob rats.

The mechanism of hearing impairment due to diabetes mellitus was examined in relation to changes in the level of the immunoreaction for the protein gene product 9.5 in the cochlea of spontaneously diabetic WBN/Kob rats. At 7 months (33 weeks) of age, when half of the males of this strain manifest diabetes, male WBN/Kob rats were divided into two groups as follows: one group consisted of prediabetic animals showing slightly decreased tolerance to glucose with a normal plasma concentration of glucose, normal urinary excretion of glucose, and functional hearing impairment (assessed in terms of elevation of hearing threshold). The second group consisted of diabetic animals with glucose intolerance, high plasma glucose level, polyuria, urinary glucose excretion, and more apparent elevation of hearing threshold. According to morphometric analysis of the spiral ganglion, the number of ganglion cells was significantly smaller in both the prediabetic and the diabetic animals than in the age-matched control Wistar rats. The staining intensity for protein gene product 9.5 was increased in some spiral ganglion cells of diabetic animals, but decreased in others according to quantitative immunohistochemical analysis. On the other hand, the immunoreactivity for protein gene product 9.5 was similar in the prediabetic animals to that in the control Wistar rats. These results suggest that numerical and immunohistochemical changes in the spiral ganglion cells reflect the onset and degree of the diabetic hearing impairment.